Yu Deng, Sida Huang, Guanming Jiang, Luyi Zhou, Alireza Nezamzadeh-Ejhieh, Jianqiang Liu and Zhikun Zhou
{"title":"Current status and prospects of MOFs loaded with H2O2-related substances for ferroptosis therapy","authors":"Yu Deng, Sida Huang, Guanming Jiang, Luyi Zhou, Alireza Nezamzadeh-Ejhieh, Jianqiang Liu and Zhikun Zhou","doi":"10.1039/D4MD00261J","DOIUrl":null,"url":null,"abstract":"<p >Ferroptosis is a programmed cell death mechanism characterized by the accumulation of iron (Fe)-dependent lipid peroxides within cells. Ferroptosis holds excellent promise in tumor therapy. Metal–organic frameworks (MOFs) offer unique advantages in tumor ferroptosis treatment due to their high porosity, excellent stability, high biocompatibility, and targeting capabilities. Inducing ferroptosis in tumor cells primarily involves the production of reactive oxygen species (ROS), like hydroxyl radicals (˙OH), through iron-mediated Fenton reactions. However, the intrinsic H<small><sub>2</sub></small>O<small><sub>2</sub></small> levels in tumor cells are often insufficient to sustain prolonged consumption, limiting therapeutic efficacy if ˙OH production is inadequate. Therefore, catalyzing or supplementing the intracellular H<small><sub>2</sub></small>O<small><sub>2</sub></small> levels in tumor cells is essential for inducing ferroptosis by nanoscale metal–organic frameworks. This article reviews the biological characteristics and molecular mechanisms of ferroptosis, introduces H<small><sub>2</sub></small>O<small><sub>2</sub></small>-related substances, and reviews MOF-based nanoscale strategies for enhancing intracellular H<small><sub>2</sub></small>O<small><sub>2</sub></small> levels in tumor cells. Finally, the challenges and prospects of this approach are discussed, aiming to provide insights into improving the effectiveness of ferroptosis induced by MOFs.</p>","PeriodicalId":88,"journal":{"name":"MedChemComm","volume":" 9","pages":" 2996-3016"},"PeriodicalIF":3.5970,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"MedChemComm","FirstCategoryId":"1085","ListUrlMain":"https://pubs.rsc.org/en/content/articlelanding/2024/md/d4md00261j","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Pharmacology, Toxicology and Pharmaceutics","Score":null,"Total":0}
引用次数: 0
Abstract
Ferroptosis is a programmed cell death mechanism characterized by the accumulation of iron (Fe)-dependent lipid peroxides within cells. Ferroptosis holds excellent promise in tumor therapy. Metal–organic frameworks (MOFs) offer unique advantages in tumor ferroptosis treatment due to their high porosity, excellent stability, high biocompatibility, and targeting capabilities. Inducing ferroptosis in tumor cells primarily involves the production of reactive oxygen species (ROS), like hydroxyl radicals (˙OH), through iron-mediated Fenton reactions. However, the intrinsic H2O2 levels in tumor cells are often insufficient to sustain prolonged consumption, limiting therapeutic efficacy if ˙OH production is inadequate. Therefore, catalyzing or supplementing the intracellular H2O2 levels in tumor cells is essential for inducing ferroptosis by nanoscale metal–organic frameworks. This article reviews the biological characteristics and molecular mechanisms of ferroptosis, introduces H2O2-related substances, and reviews MOF-based nanoscale strategies for enhancing intracellular H2O2 levels in tumor cells. Finally, the challenges and prospects of this approach are discussed, aiming to provide insights into improving the effectiveness of ferroptosis induced by MOFs.
期刊介绍:
Research and review articles in medicinal chemistry and related drug discovery science; the official journal of the European Federation for Medicinal Chemistry.
In 2020, MedChemComm will change its name to RSC Medicinal Chemistry. Issue 12, 2019 will be the last issue as MedChemComm.